Biological influence of Hakai in cancer: a 10-year review

被引：44

作者：

Aparicio, Luis A. ^{[2
]}

Valladares, Manuel ^{[1
,2
]}

Blanco, Moises ^{[1
]}

Alonso, Guillermo ^{[2
]}

Figueroa, Angelica ^{[1
]}

机构：

[1] Univ A Coruna, Translat Canc Res Grp, Inst Invest Biomed A Coruna INIBIC, Complejo Hosp,SERGAS, La Coruna 15006, Spain

[2] Univ A Coruna CHUAC, Serv Oncol Med, Complejo Hosp, La Coruna, Spain

来源：

CANCER AND METASTASIS REVIEWS | 2012年 / 31卷 / 1-2期

关键词：

Hakai; E3; ubiquitin-ligase; E-cadherin; Epithelial-mesenchymal transition; CELL-CELL-ADHESION; CADHERIN-BETA-CATENIN; WEST-NILE-VIRUS; TYROSINE PHOSPHORYLATION; ADHERENS JUNCTIONS; TUMOR ANGIOGENESIS; TRANSGENIC ADENOCARCINOMA; SRC ACTIVITY; C-CBL; PROTEIN;

D O I：

10.1007/s10555-012-9348-x

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

In order to metastasize, cancer cells must first detach from the primary tumor, migrate, invade through tissues, and attach to a second site. Hakai was discovered as an E3 ubiquitin-ligase that mediates the posttranslational downregulation of E-cadherin, a major component of adherens junctions in epithelial cells that is characterized as a potent tumor suppressor and is modulated during various processes including epithelial-mesenchymal transition. Recent data have provided evidences for novel biological functional role of Hakai during tumor progression and other diseases. Here, we will review the knowledge that has been accumulated since Hakai discovery 10 years ago and its implication in human cancer disease. We will highlight the different signaling pathways leading to the influence on Hakai and suggest its potential usefulness as therapeutic target for cancer.

引用

页码：375 / 386

页数：12

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